Pioneering Innovative Treatments for Fibrotic DiseasesCorporate Overview | Non-Confidential | August 2021

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Forward Looking Statements

This presentation contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act. These forward-looking statements include, among other things, statements regarding the clinical development pathway for CM-101; the future operations of Chemomab and its ability to successfully initiate and complete clinical trials and achieve regulatory milestones; the nature, strategy and focus of Chemomab; the development and commercial potential and potential benefits of any product candidates of Chemomab; and that the product candidates have the potential to address high unmet needs of patients with serious fibrosis-related diseases and conditions. Any statements contained in this communication that are not statements of historical fact may be deemed to be forward-looking statements. These forward-looking statements are based upon Chemomab’s current expectations. Forward-looking statements involve risks and uncertainties.

Because such statements deal with future events and are based on Chemomab’s current expectations, they are subject to various risks and uncertainties and actual results, performance or achievements of Chemomab could differ materially from those described in or implied by the statements in this presentation, including: the uncertain and time-consuming regulatory approval process; risks related to Chemomab’s ability to correctly manage its operating expenses and its expenses; Chemomab’s plans to develop and commercialize its product candidates, including CM-101; the timing of initiation of Chemomab’s planned clinical trials; the timing of the availability of data from Chemomab’s clinical trials; the timing of any planned investigational new drug application or new drug application; Chemomab’s plans to research, develop and commercialize its current and future product candidates; the clinical utility, potential benefits and market acceptance of Chemomab’s product candidates; Chemomab’s commercialization, marketing and manufacturing capabilities and strategy; Chemomab’s ability to protect its intellectual property position; and the requirement for additional capital to continue to advance these product candidates, which may not be available on favorable terms or at all. Additional risks and uncertainties relating to Chemomab’s and its business can be found under the caption “Risk Factors” and elsewhere in Chemomab’s filings and reports with the SEC. Chemomab expressly disclaims any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in Chemomab’s expectations with regard thereto or any change in events, conditions or circumstances on which any such statements are based.

This presentation (“Presentation”) is for informational purposes only and does not constitute an offer to sell, solicitation of an offer to buy, or a recommendation to purchase any equity, debt or other financial instruments of Chemomab. The data contained herein is derived from various internal and external sources. No representation is made as to the reasonableness of the assumptions made within or the accuracy or completeness of any other information contained herein. All levels, prices and spreads are historical and do not represent current market levels, prices or spreads, some or all of which may have changed since the issuance of this document. Any data on past performance, modeling contained herein is not an indication as to future performance. Chemomab assume no obligation to update the information in this Presentation. Chemomab does not accept any liability whatsoever for any losses arising from the use of this Presentation or reliance on the information contained herein. Nothing herein shall be deemed to constitute investment, legal, tax, financial, accounting or other advice. This Presentation is being provided for use only by the intended recipient.

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Clinical Differentiation

Near-Term Catalysts

Robust IP Portfolio

Focus • Discovery and development of innovative therapeutics for rare fibrotic diseases

• CM-101, a first-in-class CCL24 neutralizing mAb with confirmed anti-fibrotic MoA• Validated CCL24 as critical fibrosis target: clinical findings and experimental models• Positive Ph1b data including safety, tolerability, PK, PD and biomarker readouts

• Advancing three phase 2 clinical programs in parallel• First clinical readouts are expected during 2022 to drive multiple value inflections

• Issued CoM, multiple nationalization stage filings, worldwide patent exclusivity through 2041

Chemomab HighlightsA Clinical Stage Biotech Company

CoM- Composition of matter

Top Tier InvestorsCormorant Asset

Management

Solid Balance Sheet • Cash and equivalents of $67M as of June 30th , 2021 enabling runaway through mid 2023

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Adi Mor, PhDChief Executive Officer& Co-Founder

Stephen Squinto, PhD Chairman of the Board

Nissim Darvish, MD, PhDDirector

Joel Maryles, CFA, MBADirector

Management

Board of Directors Scientific Advisory Board

ADI MOR, PhDChief Executive Officer, Co-Founder

ARNON AHARON, MDChief Medical Officer

SHARON ELKOBI, MSc, MBAVP Business Development

MICHAL SEGAL-SALTO, PhDVP Research and Development

SHARON HASHMUELI, PhDHead of CMC and Regulatory Affairs

Prof. Marco Matucci, Cerinic, MD, PhDDirector of the Division of Rheumatology, University of Florence, Italy

Prof. Dinesh Khanna MD, MBBS, MScDirector of the Scleroderma Program, University of Michigan, Ann Arbor, Michigan, USA

Prof. Francesco Del Galdo, MD, PhDHead of the Scleroderma Program at NIHR, University of Leeds, UK

Gideon Hirschfield, MA MB PhDLily and Terry Horner Chair in Autoimmune Liver Disease, University of Toronto, Toronto General Hospital, Canada

Massimo Pinzani, MD, PhD, FRCP Sheila Sherlock Chair of Hepatology, Director UCLInstitute for Liver and Digestive Health, RFH, London, UK

Scott L. Friedman, MDThe Dean for Therapeutic Discovery and Chief, Division of Liver Diseases, Mount Sinai, NY, USA

Experienced Leadership

SIGAL FATTAL, CPAChief Financial Officer

Alan Moses, MDDirector

Claude Nicaise, MDDirector

Neil Cohen, MADirector

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Chemomab Strategy: Fibrotic Disease FranchiseAddressing Fibrotic Diseases with High Unmet Need

IV- Intravenous; SC- Subcutaneous, MoA- Mechanism of Action

TARGETINDICATION DISCOVERY PRECLINICAL

ANTI FIBROTIC MoA in LIVER FIBROSIS

PHASE 1 PHASE 2 PHASE 3

CM-101 (IV)

CM-101 (IV)

PRIMARY SCLEROSING CHOLANGITIS

SYSTEMIC SCLEROSIS

CM-101 (SC)

Orphan designation granted from FDA and EMA

Orphan designation granted from FDA and EMA

NEXT-GEN SCREENINGFIBROSIS

PROGRAM

CCL24

CCL24

CCL24

6

CCL24 is a Novel Therapeutic Target for FibrosisCritical Mediator Promoting Inflammation and Fibrosis

CCL24

CCR3

M2 Macrophages, Immune

and Epithelial cells

CCL24-secreting cells

CCL24-regulated cells

Fibroblasts (liver, lung and skin),

Immune cells and Cholangiocytes

Immune cells recruitment Fibroblasts activation

Tissue scarring, inflammatory-mediated damage, collagen deposition

Po

siti

ve

Fe

ed

ba

ck

Lo

op

✓ Dual role in promoting fibrosis

- directly activates fibroblasts

- enhances local immune cell recruitment

✓ Unique and differentiated activity

- ex vivo and in vivo data confirms unique role vs other CCLs

✓ Minor expression in healthy tissue

- significantly elevated in liver, skin, lung fibrotic tissue

- wide therapeutic margin

- correlates with disease outcome and fibrotic biomarkers

✓ Positive feedback loop potentiates tissue damage

- responsible for initiation and perpetuation of fibrosis

Organ failureDamaged tissue CCL24 Secretion

7

CCR3

Immune cells recruitment

Fibroblasts activation & proliferation

CCL24

CM-101

FibrosisInflammation

CM-101- A First in Class mAb Blocking CCL24Dual Mechanism of Action Interfering with the Core Fibrotic Pathways

CM-101 attenuates inflammation and fibrosis by inhibiting fibroblast activation and immune cell recruitment

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Source: Johns Hopkins Medicine

Primary Sclerosing Cholangitis (PSC)

o PSC is a rare, chronic bile duct inflammatory and fibrotic disease leading to end-stage liver disease and cirrhosis

o No FDA approved drug; Liver transplant is the only therapy with curative potential

o Median Survival of 10-12 years with no intervention

o ~77K patients in 7 major markets; +$1B market potential

Orphan Drug Designation granted for CM-101 in EU and US

Lazaridis et al. Primary Sclerosing Cholangitis., N Engl J Med. 2016 James H et al.Primary Sclerosing Cholangitis, Part 1: Epidemiology, Etiopathogenesis, Clinical Features, and Treatment Gastroenterology & Hepatology 20187 Major Markets – USA, 5EU (UK, Germany, France, Italy, Spain), Japan

Potentiating High Morbidity and Mortality

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CCL24 serum level in PSC patients

Healthy Liver

Collaboration with RFH, UK

PSC Liver

CC

L2

4 S

TA

ININ

G

CCL24 expression is significantly and selectively elevated in PSC livers

CCL24 level in healthy vs PSC patients' livers tissues

Strong correlation between CCL24 and fibrotic biomarkers

CCL24 Plays a Key Role in PSC PathologyTarget Validation in PSC

Chemomab’s Internal report ELF – Enhanced Liver Fibrosis; ALP – Alkaline Phosphatase

10

% F

ibro

sis

(sir

ius

red

sta

inin

g)

0

20

40

60

80

100

TAA TAA +CM-101(2.5mg/kg)

82% reduction

Col1A1Col3A1TIMP1ACTA2TGF-β

ALTASTALP

Liver enzymes

Pro-fibrotic genes

CM-101 Reduces Liver Fibrosis by 80%

Segal-Salto et al, JHEP reports 2020TAA- Thioacetamide

Reduced Liver Collagen in TAA Liver Fibrosis Rat Model Using Therapeutic DesignH

EA

LT

HY

T

AA

SIRIUS RED (COLLAGEN)

TA

A+

C

M-1

01

11

CM-101 Reduces Liver Injury and Fibrosis in PSC Cholestasis, Inflammation and fibrosis are reduced in the MDR2 Knockout Model in Mice

Chemomab’s internal report

CM-101 interferes with the core pathways that drive PSC

Mdr2 -/- Mdr2 -/- CM-101 (D8)

Mdr2 -/- Mdr2 -/- CM-101 (D8)

0.0

0.5

1.0

1.5

Exp

ressio

n (

Rea

l-ti

me P

CR

)

TIMP1 Col1a1

✱✱ ✱

CM-101 attenuates liver collagen levels and fibrotic biomarkers

CM-101 reduces cholangiocytesproliferation and monocytes recruitment

Sirius Red Macrophages (IBA1) Cholagiocytes (panck)

Md

r2 -

/-

Md

r2 -

/-

Md

r2 -

/-+

CM

-10

1

Md

r2 -

/-+

CM

-10

1

12

o Systemic Sclerosis (SSc) is a rare autoimmune rheumatic disease characterized by inflammation and fibrosis of the skin and internal organs

o There is no approved disease modifying drug; Treatments focus on managing disease symptoms (Nintedanib, Tocilizumab)

o Median Survival of 10 years - the highest mortality rate among the systemic rheumatic diseases

o ~140K patients in 7 major markets ; +$2B market potential

Orphan Drug Designation granted for CM-101 in EU and US

Systemic Sclerosis (SSc)

Global data, systemic sclerosis (scleroderma) – opportunity analysis and forecast to 2024Bergamasco et al., Clin Epidemiol. 2019; 11: 257–2737 Major Markets – USA, 5EU (UK, Germany, France, Italy, Spain), Japan

Most Lethal Among Systemic Rheumatic Diseases

Source:

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CCL24: A Critical Node Potentiating Systemic Sclerosis (SSc)Target Validation in SSc

Mor A et al., Annals of Rheumatic Diseases, 2019***p ≤0.001 BLM – Bleomycin; WT - Wild type; KO - Knock out

CCL24 Levels in Skin Tissues of SSc Patients

• Significantly overexpressed in skin of SSc

patients vs. healthy

CCL24 Levels in Serum samples of SSc patients

• Strongly elevated in diffused SSc serum

• Correlates with fibrotic biomarkers and disease progression

***SSc Skin

Collaboration with University of Florence

Healthy Skin

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CCL24 Blockade is Singularly Sufficient to Attenuate FibrosisKnocking out the CCL24 gene attenuates experimental SSc model (bleomycin)

Mor A et al., Annals of Rheumatic Diseases, 2019BLM – Bleomycin; WT - Wild type; KO – Knockout, BAL- Bronchoalveolar lavage, PBS- Phosphate-buffered saline *p ≤0.05

WT-PBS

CCL24 KO-PBS

WT-BLM

CCL24 KO-BLM

0

1

2

3

4

5

6

WT-

PBS

WT-

BLM

CCL24 KO-

PBS

CCL24 KO-

BLM

Fo

ld in

cre

ase

exp

ress

ion

α SMA expression in skin lesions

Dermal thickness

0.6

0.8

1

1.2

1.4

1.6

1.8

WT PBS WT BLM CCL24 KO-

PBS

CCL24 KO-

BLM

De

rma

l th

ick

ne

ss c

om

pa

red

to

a

ve

rag

e c

on

tro

l g

rou

ps

*

*

0

1000

2000

3000

4000

5000

# c

ells

infi

ltra

tin

g t

o B

AL

Immune cell lung infiltration

*

WT-BLM CCL24KO-BLM

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CM-101 Profoundly Reduces Skin and Lung Fibrosis in SScExperimental Models Relevant to Systemic Sclerosis Using Prevention and Therapeutic Designs

Mor et al, Annals of Rheumatoid Diseases, 2019**p ≤0.01; *p ≤0.05. BLM - bleomycin; IT - Intratracheal; SC – SubcutaneousIgG - Immunoglobulin G

Attenuates skin and lung fibrosis levels in bleomycin induced models using treatment mode

Demonstrates a dose dependent attenuation of fibrosis

Reduces lung collagen and inflammation as compared to approved drugs for lung fibrosis

Bleomycin (IT) induced lung fibrosis

0

20

40

60

80

100

Co

llage

nco

nce

ntr

atio

n (µ

g/gr

tis

sue)

Vehicle BLM BLM+CM-101

0.5mg/kg

BLM+CM-101 1mg/kg

BLM+CM-101

2.5mg/kg

BLM+lgG

**

**

Bleomycin (SC) induced dermal fibrosis

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CM-101 Holds a Robust Preclinical PackageSignificantly Attenuates Fibrosis & Inflammation Across a Wide Range of Models

Primary sclerosing cholangitis

• ANIT induced cholestasis-chronic and acute (mice)

• Bile duct ligation (rat)

• MDR2 knock-out (mice)

Systemic sclerosis

• Bleomycin-induced skin fibrosis (mice)

• Bleomycin induced lung fibrosis (mice)

Liver Fibrosis

• TAA induced liver fibrosis (rat and mice)

Nonalcoholic steatohepatitis

• STAM (mice)

• MCD diet induced NASH (mice)

Atherosclerosis

• ApoE knock out model (mice)

Proof of Concept Animal Models

CM-101 effects on fibroblasts activation

• Dermal, Hepatic and Lung fibroblast activation

• Dermal and liver fibroblast transition to myofibroblasts

• Hepatic fibroblast motility

CM-101 effects on immune cells migration and recruitment

• Dermal fibroblast migration

• Monocyte polarization

• Monocytes recruitment

Mechanism of Action

Ex-Vivo (Patient Samples)

PSC

• Biomarkers correlation

• Overexpression of CCL24 and CCR3

Systemic Sclerosis

• Fibrotic biomarkers correlation

• Disease deterioration correlation

• Overexpression of CCL24 and CCR3

NASH

• Disease severity correlation

• Overexpression of CCL24 and CCR3

In-Vivo (Knockout Animal Models)

Systemic Sclerosis

• CCL24 knock out vs. WT in Bleomycin induced skin fibrosis model (mice)

NASH

• CCL24 knock out vs. WT in MCD induced NASH (mice)

CCL24 Target Validation

• Short-term GLP in rodents

• Long-term GLP in Non-human primates

• Ex-vivo safety: ADCC, CDC, cytokine secretion

• Tissue cross reactivity

Toxicology

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• CM-101 was safe and well tolerated at all tested doses up to 10 mg/kg and for both formulations

• Average t1/2 of 19-21 days (for IV and SC), supports long interval administration once every 2-4 weeks

• Dose dependent target engagement measured by serum CCL24 levels

• Comparable target engagement & PK Profiles for the SC and IV formulations

Double-Blind, Randomized Escalating Dose (N=32)

CM-101 0.75 mg/kg IV or placebo

CM-101 2.5 mg/kg IV or placebo

CM-101 5 mg/kg IV or placebo

CM-101 10 mg/kg IV or placebo

Double-Blind, Randomized Single Dose (N=8)

CM-101 5 mg/kg SC or placebo

IV Phase 1

End of 42 days follow-up period

SC Phase 1

End of 42 days follow-up periodScreening period (up to 28 days)

Follow-up period (6 weeks)

n=40 healthy volunteers

CM-101 is Safe & Well Tolerated in Healthy Volunteers

IV - Intravenous; SC - Subcutaneous

Phase 1a Single Administration study

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• Tested doses - 2.5 mg/kg IV infusion and 5 mg/kg SC injection

• 5 repeated administrations per patient; Q3W

• Primary endpoint - safety and tolerability

Wk 15End of treatment

Wk 18End of study

Double-Blind, Randomized Escalating Dose (N=16)

CM-101 2.5 mg/kg IV or placebo

CM-101 5 mg/kg SC or placebo

Phase 1b

Day 0Randomization

Study Design

• Study population- NAFLD patients with normal liver function

• Multiple CM-101 administrations were safe and well tolerated using both IV and SC formulations

• Favorable t1/2, supports long dosing interval (Q2W - Q4W)

• Dose dependent PK and target engagement

Ph1b Demonstrates Safety & Tolerability Along 15 Weeks TreatmentPhase 1b Multiple Administration Study in NAFLD Patients

IV - Intravenous; SC – Subcutaneous; Wk - week

19

0 21 42 63 84 105 126

0

20

40

60

0

50

100

150

200

250

Time (days)

CM

-10

1 (

ug

/mL

)

CC

L24 (fo

ld c

ha

ng

e %

)

0 21 42 63 84 105 126

0

5

10

15

20

25

0

50

100

150

Time (days)

CM

-10

1 (

ug

/mL

)

CC

L24 (fo

ld c

ha

ng

e %

)

CM-101

CCL24 (Target Eng.)

First evidence for an anti fibrotic effect in human supported by dose dependent PK-PD

CM-101 Target Engagement & Anti-Fibrotic Mechanism Human Confirmation for CM-101 Anti-Fibrotic Mechanism of Action

ProC4-Procollagen 4TIMP1- metallopeptidase inhibitor 1EOT-End of Treatment

PK-PD

PK-PD 2.5mg/kg IV

0 21 42 63 84 105 126

0

5

10

15

20

25

0

50

100

150

Time (days)

CM

-101

(

g/m

L)

CC

L24 (fo

ld c

ha

ng

e %

)

CM-101

CCL24 (Target Eng.)

PK-PD 5mg/kg SC

Liv

er

Sti

ffn

ess

R

ela

tive

ch

an

ge

fro

m b

ase

line

(%

)

Nordic Biosciences , Denmark

Fibrotic Biomarkers*

-30

-15

0

15

30

Liv

er

sti

ffn

ess

(%

ch

an

ge f

rom

base

lin

e)

FibroScan™

CM

-101

Pla

cebo

-2.5

-2.0

-1.5

-1.0

-0.5

0.0

0.5

1.0

Liv

er

sti

ffn

es

s (

kP

a) CM-101

Placebo

ProC4 TIMP1

-20

-10

0

10

20

-20

-10

0

10

CM-101

Placebo

*Concordant results across 6 relevant fibrotic markers

TIMP1

Elastography

CM

-101

Pla

cebo

-2.5

-2.0

-1.5

-1.0

-0.5

0.0

0.5

1.0

Liv

er

sti

ffn

es

s (

kP

a) CM-101

Placebo

Re

lati

ve c

ha

ng

e f

rom

ba

selin

e (

%)

EOT

EOT

20

CM-101 Clinical Development Plan and Key Catalysts

FPI- First patient in, LPI - Last patient in, IA - Interim assessment

POC - Proof of Concept, IV -Intravenous, SC – Subcutaneous,

MoA- Mechanism of Action

*NCT04595825

Advancing in Parallel Three Phase II Clinical Programs

Status 2021 2022 2023

Primary Sclerosing Cholangitis

EnrollingTop line data expected in 2H2022

Systemic Sclerosis

Initiation expected in 1Q2022

Liver FibrosisProof of MoAusing SC formulation

EnrollingTop line data expected in 1H2022

Phase II: 15wk treatment*Randomized placebo-controlled;Europe and Israel study sites

Phase II: 24-48 wk treatmentRandomized placebo-controlled;US & Europe study sites

Phase IIa: 14 wk treatmentRandomized placebo-controlled;Israel study sites

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Chemomab, Fighting Fibrosis Across Indications Pioneering Innovative Treatment for Fibrosis-Related Diseases with High Unmet Need

IV – Intravenous; SC - Subcutaneous

Chemomab

• Clinical stage company entering Ph2 trials in

multiple fibrotic indications with high unmet need

• Substantial near term value inflection points

• Strong leadership with proven track record

PK & Mode of Administration

• Optimal PK for both SC and IV

formulations

• Comparable Exposure levels and

target engagement using both

formulations

Efficacy

• First anti-fibrotic evidence in

patients

• Significant anti-fibrotic effects

across multiple in vivo, ex vivo

and in vitro models

CM-101

• First-in-class mAb blocking CCL24

• Novel and differentiated dual anti-fibrotic and anti-inflammatory MoA

• SC and IV Formulation; Contract manufactured via reputable & established CMO

• Strong IP protection

Safety

• Favorable safety and tolerability

that support chronic treatment

based on toxicology, Phase Ia and

Phase Ib clinical trials

Presentation name

Thank You